Dr. Doerr’s Diagnostic Dilemma
28 y/o M w/ hx of Bipolar (noncompliant with lithium) who presents with cc of myalgias and itchy painful penile rash over the last few days. Initial FSG 600s. On ROS pt noted to have polyuria, polydipsia over the last few weeks and weight gain ~ 80lbs over the last year. Has maternal history of Type II diabetes.
Exam revealed mild HTN, BMI of 45, significant abdominal girth, non-cushingoid exam, erythematous penile frenulum, no discharge, ulcers or pelvic lympadenopathy. Initial labs revealed hemoconcentration with Albumin of 4.7, anion gap 15 with ph of 7.35 on peripheral VBG, CK in the 3000s, TG in 2000s, HDL 20 and UA +2 Blood, no RBCs and 2+ Ketones.
Pt was diagnosed with volume depletion, DKA & myopathy in the setting of Type II Diabetes. He was fluid resuscitated with normal saline and glucose controlled with subq insulin. Over the next 72 hours his glucose steadily improved to 200-300 but his acidosis worsened to 7.31/28/14/93/97% on ABG with an Anion Gap acidosis per Chem 7 (Na 127 CO2 6, Cl100, ag=21) and a non-anion gap acidosis per ABG (Na 137 Cl 105 C02 15, ag=12). UA still has + ketones, Urine Anion Gap of 40.
What should we believe? Is this an RTA or just resolving DKA superimposed on a non-gap acidosis from NaCl administration?
Why is this Type II diabetic producing ketones? Was the penile rash the stress trigger that pushed him into this DKA picture.
Is muscle damage common in DKA and do we understand why?
Case Study: Diabetic Ketoacidosis “Look under the Sheets” & “Tea Colored Urine in Ketoacidosis”
Dr. Borkan’s Response:The most likely etiology for the hyperchloremic non-gap met. acidosis is the persistent urinary excretion of keto-acids that are bicarbonate equivalents; in this case, the persistence of urinary ketones and the prolonged time frame (72 hrs) could explain the hyperCl picture due to “bicarbonaturia” (see ref below)
It is also possible that massive (>L 8/day) of normal saline could explain this picture (but I doubt that this much fluids was administered).
RTA would be difficult to distinguish from the effect of ketonuria-but persistent RTA has been reported in a pt with DKA and DM that lasted 7 mos.
The treatment is to stop the ketonuria, most likely representing mild DKA, since the anion gap on admit was only 15 and the patient was predominantly hyperosmolar.
I cannot easily explain why the serum and ABG lytes showed anion-gap vs. gap acidosis. The Na frm each lab test is quite different and could reflect rapid and large changes intake serum glucose when the studies were obtained….
Or this is lab error as it would be quite unusual to have worsening acidosis (falling bicarb) with a progressive increase in anion gap (15 to 21) as the glucose was being effectively reduced from 600 to 2-300 mg% range.
1. Gamblin, G.T., et al., Diabetic ketoacidosis presenting with a normal anion gap. Am J Med, 1986. 80(4): p. 758-60.
2. Giammarco, R., et al., Renal tubular acidosis during therapy for diabetic ketoacidosis. Can Med Assoc J, 1975. 112(4): p. 463-6.
3. Oh, M.S., M.A. Banerji, and H.J. Carroll, The mechanism of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. Diabetes, 1981. 30(4): p. 310-3.